Impaired microvascular reactivity in post-COVID-19 syndrome is independent of cardiorespiratory fitness

Current evidence demonstrates that patients that suffer from long-term SARS-CoV-2 symptoms (i.e., post-COVID-19 syndrome, PCS) often present muscle fatigue and dyspnea. This is discussed to be a result of vascular dysfunction and oxidative stress triggered by the infection. However, its effects on the microvasculature remains unknown. 62 participants (61.3% women) were recruited (50.0±11.8 yr, body mass index (BMI) 27.6±5.3 kg·m -2 , maximal oxygen uptake (V̇O 2max ) 26.2±9.4 mL·kg -1 ·min -1 ) from the EPILOC (Epidemiology and clinical characteristics of PCS) phase 2 study. Participants were divided into either a case group (patients with new or prolonged symptoms and impaired general health or work ability compatible with persistent PCS) or control group (symptom-free age-sex matched patients with uneventful recovery after COVID-19). The brachial-ankle pulse wave velocity (baPWV) was assessed via BOSO-ABI system100. To evaluate the microvascular function, a tissue oxygen saturation (StO 2 ) reperfusion rate assessment using near-infrared spectroscopy was performed on the flexor digitorum superficialis muscle. No significant statistical differences were observed between the case and control groups in age, BMI, and baPWV (p>0.05). The control group achieved a greater V̇O 2max than the case group (p=0.02). After adjusting for V̇O 2max , a significant effect of group (F (1,52) =5.28, p=0.026) in microvascular function was observed, with the case group presenting lower values than the control group (=-0.53, p=0.02). No a priori power calculation was performed – post-hoc sensitivity analysis indicated a minimum detectable effect of Cohen's d=0.72, and secondary outcomes should be interpreted cautiously. Our results indicate a reduced microvascular function in patients with PCS, as compared with the control group. Such impairment may be linked to the prolonged symptoms experienced by patients, causing capillary flow disturbance and, subsequently, limiting muscle oxygen uptake.